ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Complement is involved in inflammation and in the optimization of adaptive responses. Abnormalities in the complement system have been associated with autoimmunity, especially systemic lupus erythematosus. A paradoxic relation exits between complement and lupus. Complement-mediated tissue damage is accepted as a mechanism in disease pathophysiology. Conversely, complement exerts a protective effect in disease development. The theoretic framework explaining this protective influence involves the adequate disposal of apoptotic material by classic pathway components. Inadequate clearance of apoptotic material may evoke a proinflammatory autoimmune response. This conceptual model is substantiated by studies indicating that complement receptor genes are within major susceptibility loci of systemic lupus erythematosus, that functional and structural abnormalities in these receptors are found in lupus mouse models, and that genetic polymorphism of lectin pathway genes correlates with increased risk of disease development. Finally, new diagnostic and therapeutic modalities based on complement regulation have been described in the past year.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by the production of autoantibodies and the development of immune complex glomerulonephritis. Lupus nephritis (LN) remains a leading cause of morbidity and mortality in SLE. As a result, defining pathogenetic mediators in LN remains a major research effort. Progression to LN in SLE is dependent on the host breaking immune tolerance and forming autoantibodies that deposit in the kidney. A variety of predisposing factors in the host must then be present for this event to result in renal pathology. In this article, the authors review recent reports that advance our understanding of LN disease mediators, from autoantibody production and immune complex deposition to end stage fibrosis.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Blood vessel homeostasis involves a complex interplay between inflammatory signals, hormones, and other mediators. Recent research suggests that although atherosclerosis is primarily a problem of impaired lipid regulation, the very processes of cholesterol and triglyceride metabolism are intrinsically tied to inflammatory and hormonal regulatory signals. Similarities between inflammatory and endocrine disturbances in systemic lupus and the predicted consequences for vascular regulation help explain the high incidence of premature atherosclerosis in lupus. Atherosclerosis in systemic lupus, then, may be a consequence of imbalances in what are intrinsic homeostatic mechanisms, rather than a result of externally superimposed pathologic changes.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Neuropsychiatric syndromes associated with systemic lupus erythematosus are common, but diverse in etiology and presentation. Cognitive dysfunction is prevalent among these syndromes, but exhibit a significant degree of heterogeneity both within and between patient variability. Earlier studies of SLE-associated cognitive dysfunction addressed its identification and description. Common associations were repeatedly acknowledged, including concomitant or past neuropsychiatric disease, use of corticosteroids, disease activity, emotional disturbance, and antiphospholipid antibodies. The past several years have focused more on elucidating the relative strengths of various risk associations, patterns of cognitive abnormalities, both cross-sectionally and longitudinally (ie, clinical course), and novel means to identify cognitive impairment, both functionally and biologically.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

The last significant breakthrough in the treatment of systemic lupus erythematosus (SLE) was the use of cyclophosphamide and methylprednisolone in the treatment of lupus nephritis. Recent advances in immunology, oncology, and endocrinology have resulted in many potential therapies for SLE. These therapies include new immunosuppressants, biologic medications, tolerizing agents, immunoablation techniques, and hormonal medications. Each of these approaches will be discussed in this review. Some therapies are currently in use in clinical rheumatology practice (mycophenolate mofetil) and others are entering phase I trials (anti-BLyS monoclonal antibody). While some of these new therapies target specific inflammatory mechanisms in SLE (anti-CD40L monoclonal antibody), others work by nonspecific inhibition of the immune system (immunoablation).

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

B lymphocyte stimulator (BLyS) protein is among the novel tumor necrosis factor (TNF) ligands and receptor superfamily members recently described. BLyS protein can promote B cell survival, expansion, and differentiation bothin vitroandin vivo. Constitutive overexpression of BLyS protein can result in systemic lupus erythematosus (SLE)-like disease in mice, and circulating levels of BLyS protein are elevated in a subset of human SLE patients. Treatment of SLE mice with a BLyS protein antagonist ameliorates disease progression and enhances survival. By inference, BLyS protein may also play an important contributory role in pathogenesis and/or propagation of human SLE and becomes a legitimate candidate target for antagonist biologic agents.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

This article reviews recent publications related to the classification and treatment of juvenile spondyloarthropathies. We have included studies on adult onset spondyloarthropathies that are particularly relevant to childhood onset disease. Significant questions concerning classification of juvenile spondyloarthropathies remain unresolved. Diagnostic criteria that are both sensitive and specific for identifying undifferentiated spondyloarthropathies in adults have been developed, and while separate criteria have been proposed for juvenile onset disease, they remain to be validated. The most significant recent advances have occurred in the area of treatment. A small number of studies suggest that bisphosphonates such as pamidronate may be efficacious. Several studies using the TNF inhibitors infliximab and etanercept suggest that these agents hold great promise for ameliorating symptoms and improving function, while long-term effects on disease progression remain to be evaluated.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

In contrast to adult rheumatoid arthritis, hips are commonly affected joints in severe, destructive, juvenile rheumatoid arthritis (JRA). Hip disease develops in 30 to 50% of children with JRA. Because of the importance of the hip joint in weight bearing the advent of hip disease in a child with JRA warns of future disability [1••,2]. The challenges for the clinician are to prevent significant hip involvement, to halt further damage when hip disease is noted, and in the event that conservative treatment fails, to guide the child and family through hip arthroplasty and rehabilitation. Recent trends suggest that today's more aggressive treatment approach and more effective drugs are resulting in fewer children with JRA developing into severe hip disease requiring hip surgery. Similarly, with improvements in orthopedic surgery, the results of hip arthroplasty have improved.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID